Background: Circular RNAs play an important regulatory role in the occurrence and development of nerve damage and related diseases, but there is little research on non-coding RNAs in heat sickness, especially circRNAs, and there has been no report on the mechanism of fever progression.
Methods: 1. Mice were randomly divided into a control group, a heat radiation disease 0.8 h group (HS 0.8), 8 h group (HS 8), 24 h group (HS 24). By establishing a mouse model of heat shock (HS), heat-damaged brain tissue was obtained, microglia were isolated. 2. QPCR was used to detect M1 and M2 marker molecules in microglia, and to evaluate the polarization direction and type of microglia. 3. The expression level of circhipk3 in microglial cells, and the effect of circhipk3 on microglial polarization was determined by determining the expression of circhipk3 in microglial cells.
Results: The expressions of CD45 and CD11-b in the HS 8 group were significantly higher than those in the normal group, while the expressions of CD45 and CD11-b in the HS 24 group were significantly lower than those in the HS 8 group. At the same time, the expression of CD206, FIZZ, and Arg1 in the HS 8 group began to increase compared with the normal group, while CD206, FIZZ, and Arg1 in the HS 24 group significantly increased when compared with the normal group. Circhipk3 mimics significantly increased the expression of Arg1 and inhibited the expressions of CD45 and HO-1, while the circhipk3 inhibitor promoted the expressions of CD45 and HO-1 and inhibited the expression of Arg1.
Conclusion: Microglial cells were the main M1-type in early neurological injury of heat radiation disease. HO-1 may be one of the microglial M1-type markers. The high expression of circhipk3 in microglial cells mainly promoted its transformation to the M2 type.